Select Committee on Environment, Food and Rural Affairs Minutes of Evidence

Examination of Witnesses (Questions 20-39)



  20. Does that give an indication that further research work needs to be done in this area? I know it is a Department of Health issue.
  (Dr Bailey) It is a Department of Health issue, yes.

  21. What is your understanding of it?
  (Dr Bailey) I am afraid I do not know whether or not the Department of Health are funding any work in this particular area.

  22. You told us earlier on that there was a whole range of research work going on, and that you were happy to fund research provided you found there was some benefit. Can you just outline what the main threads of the research are that the Department is funding?
  (Dr Bailey) Yes. The DEFRA research programme is divided into four main areas. There is some overlap between them, but we are doing quite a lot of work in relation to the epidemiology of the disease. We are also looking at transmission of the disease. (When I say "the disease", I really should say two diseases, BSE and scrapie, because we are funding both work on BSE and on scrapie.) We also have quite a large programme on diagnostic developments, because clearly that is a key area. There is pathogenesis, that is, looking at the development of the disease in the animal. The work on pathogenesis has been incredibly important in determining which tissues in the animal become infected and at what stages they become infected. That has been the basis of most of the control measures that have been put in place both within the UK and within Europe.

  23. One of the popular myths from the Daily Mail is that intensive farming really is the cause of all health problems. Does any of the work that you have just outlined overlap with that?
  (Dr Bailey) The work that I have just described to you is the work that is funded in the TSE area by the Department, and clearly that does not represent the whole of DEFRA's research programme. I am afraid I do not have information on the rest of DEFRA's research programme. If you wish to have further information on that, we would need to provide you with some written comments.

  24. It would be very helpful if you could write to us on that, because one of the urban myths at the moment is that intensive farming by definition leads to disease, and I have heard it said that intensive farming has led to BSE. There may not be any proof of that at all, but it would be very helpful if you could outline whether any of the work the Department funds looks at that.
  (Dr Nash) There is a sort of connection, an indirect connection, in the link with BSE and the consumption of meat and bonemeal. For example, there has been a much higher prevalence in the dairy cattle that are more intensively fed than beef cattle, but it is not a necessary connection, of course, because we have been able to do something about it. Nevertheless, there is a sort of link there.


  25. You said earlier that you were quite happy to examine heretical views—you did not use that phrase—that if people were coming at it from a different angle, you were interested in exploring those views because we did not have the definitive solution and there was just the odd chance that this stray particle might split the atom, as it were. I have had a meeting with Professor Ebringer, and I do not pretend that I understand the science expertly. I mentioned earlier on that his contention is that BSE is caused by an auto-immune response to the common orgasm Acinetobacter, it cannot be transmitted to humans, and he is trying to develop a diagnostic test for BSE in live animals. You said you had looked at this and decided it was not possible to pursue that because it seriously challenged the prion hypothesis. What was the basis of that conclusion?
  (Dr Bailey) There were a number of reasons. Part of what Professor Ebringer said is to do with the fact that if you inject brain material into animals from brains that are not suffering from BSE, you can get a neurological disorder, and this is to do with an immune response, but in fact, the pathology of the disease, what it looks like when you look at the brains, is totally different from TSE. That was one of their reasons. I suppose the most compelling reason is that Professor Ebringer's theory is based on the fact that there has to be an immune response, and there has been some scientific work done in mice where the immune response has been destroyed, and you can still transmit TSEs to mice who have no immune system, which means that you do not need an immune system for the transmission of TSEs, and therefore it does not support the hypothesis that what is happening is that the immune response is destroying the brain, because there are proteins that mimic the proteins in this bacteria, Acinetobacter, which Professor Ebringer believes. So the evidence is quite compelling, and I think it is true to say that it is not just SEAC that have adopted this view. Professor Horn also considered this theory, and the scientists on his Committee also thought it was not a plausible theory, and they, as I said, are not necessarily experts in TSEs. In addition to that, the EU Scientific Steering Committee also considered this when they did their review of the origin, and they are a different group of scientists, and indeed the Phillips inquiry also came to the same view. So there are four different groups of people who have looked at this who do not believe it is a plausible hypothesis.

  26. So in terms of decisions on funding of research projects, for example, you have come to the conclusion that this is a dead end as far as the discovery of the origins of BSE are concerned?
  (Dr Bailey) Yes.

Mr Todd

  27. You said that very few cattle had shown evidence of the disease before 30 months. How many have?
  (Dr Bailey) I am sorry. We will have to let you have a note on that.

  28. If we take it that the 30-month rule was devised on the basis that the disease virtually always did not show itself until that age, we assume that the animal feed restrictions were in place soundly as from 1 August 1996, but we have gradually discovered that other factors must be involved in this because, of course, animals born more than 30 months after that feed control date have developed the disease. What explanations do we have for that?
  (Dr Nash) First of all, we have found out that there are 81 cases in animals lower than 30 months out of 180,000.

  29. That is not a particularly small amount. But we need to put that in the context that there are some European countries where 81 cases of any kind would be regarded as a very large number. Can you give us a profile—you will not be able to do it now—of when they developed the disease, whether it was 29 months or at a much younger age?
  (Dr Nash) Off the top of my head, I cannot, but we can let you have those statistics. Turning back to your question, first of all, before asking Peter to go into the veterinary investigations into the cases born after 1 August 1996 and the provisional conclusions we have reached, there are 20 such cases in the UK so far, 17 in Great Britain and three in Northern Ireland. Of the 17 in Great Britain, roughly half have become apparent through normal surveillance and the other half through our active testing programme. Of the cases that have come to light as a result of the active testing programme, all have been in the casualty cattle survey, which is quite interesting. The other thing I should say is that Professor Wilesmith, an epidemiologist at VLA, has been looking into the characteristics of not the whole of the 20, because we have only recently learned about some of them, but the first 11 GB cases, I think it is, and is hoping to publish a short paper fairly soon on this. All I would say at this stage is that in the case of what we call the BAB cases, which are cases born after the original feed ban of July 1998, the single risk factor was the ratio of pigs and cattle. In other words, there was a strong cross-contamination. That was the clear argument, and that seems to have been demonstrated subsequently. In the case of at least these first 11—and, of course, it is a very small number, so we must not be too clear about it—there is no such link. In fact, very tentatively, one would say that the cases are more linked to dairy cows or to the number of cattle. There is certainly no link with the pigs.
  (Mr Soul) Focusing on animals born after August 1996, which of course was the date when we had completed our feed recall system, and we believe it was the date from which the reinforced feed ban should have been as secure as it has been possible to make it, we have had this small number of cases born after that, and of course, the big question is: where they have got the disease from. We think there are four main possibilities: maternal transmission; environmental contamination; horizontal transmission; and feedborne disease, some method of continuation of the feedborne problem that we are confident caused the former epidemic. To summarise briefly, because of the fact that a number of dams in these cases are still alive, we think that maternal transmission is certainly not a likely possibility in a significant number of these cases. It is not a common factor for all of them. It is a possibility in a few of them, but again, only a possibility. Environmental contamination we have looked into very thoroughly and we do not really think there is any likelihood that that is significant, and certainly when you look at the whole of the epidemic, it does not seem to have featured as something which has kept the epidemic going. Horizontal transmission—again, there are good reasons why this does not seem very likely. A number of these cases are the first cases on these farms, so we have had to give that a lower consideration, which means that we come back again to foodborne transmission. The question is: is there still some infectivity in the system out there despite all our efforts? Is some coming in from abroad? After all, we know that back in 1996-97 there was infectivity circulating in Europe. There is pretty well free trade in most commodities between Europe and us, so are we subject to the same causes that have caused disease in France and Germany, etc? That is a distinct possibility that we have to investigate as thoroughly as we possibly can. Of course, it is extremely difficult; we are going back a number of years, and to try and get evidence of what happened in detail back then is very difficult, but those are the areas that we are looking at.

  30. Would it not be fair to say that research into this aspect ought to be given the highest priority, examining the outbreak and its implications? From all your answers, the simple answer is we do not know. You have run through all of the options, and none of them seem particularly attractive or likely as explanations of the continuing tail of this disease in this country.
  (Mr Soul) Yes. Research is going on into some of these areas. Environmental contamination is a possibility for example. We have commissioned research into that, but it is hard to see how we could construct a research project to identify what caused the disease back in 1996. It is more a question of investigating it.

  31. But these cases are continuing to occur, are they not, and in some cases in animals born significantly after 1996?
  (Mr Soul) Yes.

  32. We are not going back into the dark ages of time.
  (Mr Soul) That is right, and we are investigating those. Perhaps with some of the more recent ones, we stand a better chance of making a connection. It seems quite likely that, if what I have said is true, we will continue to get a small number of cases until something changed, and what changed, of course, was that a feed ban came in throughout the whole of Europe with effect from 1 January 2001. So it may well be that we will not see a significant change in this small number of cases, this long tail going on, in younger animals until, say, five years after that date.

  33. Does this indicate that the 30-month rule ought to remain in place in terms of human health protection for quite some considerable time to come?
  (Dr Nash) The Food Standards Agency is responsible for policy on the over 30 month rule, and they have just begun a review of the rule which is likely to conclude around the end of the year. I would not really like to predict what that review is going to conclude.

  34. You have presumably given them some advice.
  (Dr Nash) No. A key element in that review will be the risk assessments, which have yet to be done. I think it is very important to have thorough and independent risk assessments to establish the actual level of risk.

  35. None of you are making any submissions about that process.
  (Dr Nash) We will certainly provide information because one of the key elements going into the risk assessments will be the testing results. Since last July we have organised the testing of about 220,000 animals in the UK for BSE, and there is a great deal of information there which will certainly feed into the review.

  36. Finally, the 20 cases you have identified of animals born after August 1996—is that in line with the expectations of those who predicted the path of this disease, or greater than or less?
  (Dr Nash) It is in line. It is a little below. The Imperial College Group, then the Oxford Group, made forecasts of the number of cases we should expect born after August 1996 on the assumption that there was 10 per cent maternal transmission.

  37. Although we are hearing that that may well not be the reason.
  (Dr Nash) That is right. The numbers that we would have had, had we had 10 per cent maternal transmission, would have been slightly greater than the numbers we have actually had. But you are perfectly right; we do not think maternal transmission is the cause of certainly the majority of these cases, if any of these cases.

Diana Organ

  38. Are these 20 cattle that have been born after 1 August 1996 showing the disease in the early part of their life or are they at 27, 28, 29 months when they show it? I wonder if you can tell me the distribution of when they are occurring since 1996. Have they come recently, in this year, or is it because you consider that the most likely case is from feedborne transmission? Are they very close to and leading up to the time when there was a feed ban across Europe? I am looking for the pattern of them and when they are exhibiting themselves.
  (Mr Soul) They are all over 30 months. That is a key point. They are not less than 30 months when they are either going down with the disease or where they have been found as a consequence of the active surveillance programme.

David Taylor

  39. What is the youngest age?
  (Mr Soul) 31 months, a Northern Ireland case. That is actually very interesting because that is really an outlier in this group. It is unusual in that it seems relatively so young, and the working assumption we would have is that it must have had a fairly heavy exposure, presumably at a fairly young age, to have gone down with the disease so young. The average age throughout the whole epidemic is increasing. It was five years, it is now more like six years, and we think that is because the exposure that they were subject to has been declining as a consequence of the feed bans.

previous page contents next page

House of Commons home page Parliament home page House of Lords home page search page enquiries index

© Parliamentary copyright 2002
Prepared 4 July 2002